Transcriptomic analysis of myosin IIa-deficient B cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE113114 | GEO | 2018/04/14
REPOSITORIES: GEO
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Project description:Transcriptomic analysis of myosin IIa-deficient B cells
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Project description:The Borg5/Cdc42EP family comprises septin binding proteins, which are known to participate in septin-dependent stress fiber formation. We show here that epithelial Borg5/Cdc42Ep1 restrains stress fibers instead. Borg5 decorates septin filament-aligned thin F-actin filaments under the nucleus of MDCK cells, which in Borg5 depleted cells are replaced by thick stellate stress fibers. These associate with either cell-substratum- or cell-cell- adhesions, increasing tension on E-cadherin based junctions and causing MDCK cells to undergo collective streaming. We identified two known septin partners, Myosin-IIA and alpha Actinin 4 (ACTN4), among proteins that co isolated with Borg5 from MDCK lysates. We found that Borg5 binds Myosin-IIA and ACTN4 directly and negatively regulates their F-actin association. Since both septin partners along with Septins 2 and 9 were furthermore required for the Borg5 depletion-induced F actin phenotype, we propose that Borg5 prevents stellate stress fiber formation by counteracting septin dependent ACTN4 and Myosin IIA activities. The mass spectrometry raw files and search results for Borg 5 affinity purifications are deposited here.
| MSV000092958 | MassIVE
Project description:To evaluate potential therapeutic benefits from dual targeting of MYC and class IIa HDACs, we assessed the treatment efficacy of MYCi plus class IIa HDACi across 18 NSCLC cell lines, 10 of which demonstrated substantial reduction of cell viability upon combination treatment. RNA sequencing on treated cell lines identified large-scale transcriptional shifts facilitated by combination treatment, including suppression of MYC, cell cycle, and mitochondrial pathways. ATAC-sequencing showed chromatin structure changes in genomic regions involved in cell cycle progression and inflammatory signaling. Furthermore, G1/S arrest and elevated mitochondrial ROS levels in combination drug-treated cells were confirmed using flow cytometry. Concordant with the role of MYC as a key cell cycle regulator, MYC protein levels were decreased in the combination treatment group as compared to the vehicle or mono-treatment groups. In summary, we define here a novel drug paradigm combining MYC and class IIa HDAC inhibitors, which potentiates anti-tumor efficacy in NSCLC via MYC depletion and oxidative stress.
2025-04-23 | GSE281767 | GEO
Project description:To evaluate potential therapeutic benefits from dual targeting of MYC and class IIa HDACs, we assessed the treatment efficacy of MYCi plus class IIa HDACi across 18 NSCLC cell lines, 10 of which demonstrated substantial reduction of cell viability upon combination treatment. RNA sequencing on treated cell lines identified large-scale transcriptional shifts facilitated by combination treatment, including suppression of MYC, cell cycle, and mitochondrial pathways. ATAC-sequencing showed chromatin structure changes in genomic regions involved in cell cycle progression and inflammatory signaling. Furthermore, G1/S arrest and elevated mitochondrial ROS levels in combination drug-treated cells were confirmed using flow cytometry. Concordant with the role of MYC as a key cell cycle regulator, MYC protein levels were decreased in the combination treatment group as compared to the vehicle or mono-treatment groups. In summary, we define here a novel drug paradigm combining MYC and class IIa HDAC inhibitors, which potentiates anti-tumor efficacy in NSCLC via MYC depletion and oxidative stress.
2025-04-23 | GSE281766 | GEO
Project description:To evaluate potential therapeutic benefits from dual targeting of MYC and class IIa HDACs, we assessed the treatment efficacy of MYCi plus class IIa HDACi across 18 NSCLC cell lines, 10 of which demonstrated substantial reduction of cell viability upon combination treatment. RNA sequencing on treated cell lines identified large-scale transcriptional shifts facilitated by combination treatment, including suppression of MYC, cell cycle, and mitochondrial pathways. ATAC-sequencing showed chromatin structure changes in genomic regions involved in cell cycle progression and inflammatory signaling. Furthermore, G1/S arrest and elevated mitochondrial ROS levels in combination drug-treated cells were confirmed using flow cytometry. Concordant with the role of MYC as a key cell cycle regulator, MYC protein levels were decreased in the combination treatment group as compared to the vehicle or mono-treatment groups. In summary, we define here a novel drug paradigm combining MYC and class IIa HDAC inhibitors, which potentiates anti-tumor efficacy in NSCLC via MYC depletion and oxidative stress.
2025-04-23 | GSE281764 | GEO
Project description:To evaluate potential therapeutic benefits from dual targeting of MYC and class IIa HDACs, we assessed the treatment efficacy of MYCi plus class IIa HDACi across 18 NSCLC cell lines, 10 of which demonstrated substantial reduction of cell viability upon combination treatment. RNA sequencing on treated cell lines identified large-scale transcriptional shifts facilitated by combination treatment, including suppression of MYC, cell cycle, and mitochondrial pathways. ATAC-sequencing showed chromatin structure changes in genomic regions involved in cell cycle progression and inflammatory signaling. Furthermore, G1/S arrest and elevated mitochondrial ROS levels in combination drug-treated cells were confirmed using flow cytometry. Concordant with the role of MYC as a key cell cycle regulator, MYC protein levels were decreased in the combination treatment group as compared to the vehicle or mono-treatment groups. In summary, we define here a novel drug paradigm combining MYC and class IIa HDAC inhibitors, which potentiates anti-tumor efficacy in NSCLC via MYC depletion and oxidative stress.
2025-04-23 | GSE279134 | GEO
Project description:To evaluate potential therapeutic benefits from dual targeting of MYC and class IIa HDACs, we assessed the treatment efficacy of MYCi plus class IIa HDACi across 18 NSCLC cell lines, 10 of which demonstrated substantial reduction of cell viability upon combination treatment. RNA sequencing on treated cell lines identified large-scale transcriptional shifts facilitated by combination treatment, including suppression of MYC, cell cycle, and mitochondrial pathways. ATAC-sequencing showed chromatin structure changes in genomic regions involved in cell cycle progression and inflammatory signaling. Furthermore, G1/S arrest and elevated mitochondrial ROS levels in combination drug-treated cells were confirmed using flow cytometry. Concordant with the role of MYC as a key cell cycle regulator, MYC protein levels were decreased in the combination treatment group as compared to the vehicle or mono-treatment groups. In summary, we define here a novel drug paradigm combining MYC and class IIa HDAC inhibitors, which potentiates anti-tumor efficacy in NSCLC via MYC depletion and oxidative stress.
2025-04-23 | GSE279133 | GEO
Project description:Congenital myopathies are rare genetic muscle diseases notably due to mutations in the MYH2 gene. Here we assessed their myosin heavy chain post-translational modifications. For that, we purified beta/slow and type IIa myosin heavy chains from limb muscles of five patients and five healthy controls. We then ran a LC/MS analysis.
2023-01-30 | PXD039178 | Pride
Project description:In addition to altered gene expression, pathological cytoskeletal dynamics in the axon are another key intrinsic barrier for axon regeneration in the central nervous system (CNS). Here we showed that knocking out myosin IIA/B in retinal ganglion cells alone either before or after optic nerve crush induced significant optic nerve regeneration. Combined Lin28a overexpression and myosin IIA/B knockout led to additive promoting effect and long-distance axon regeneration. Immunostaining, RNA sequencing and western blot analyses revealed that myosin II deletion did not affect known axon regeneration signaling pathways or the expression of regeneration associated genes. Instead, it abolished the retraction bulb formation and significantly enhanced the axon extension efficiency. The study provided clear evidence that directly targeting neuronal cytoskeleton was sufficient to induce significant CNS axon regeneration, and combining altered gene expression in the soma and modified cytoskeletal dynamics in the axon was a promising approach for long-distance CNS axon regeneration
2020-03-24 | GSE147400 | GEO
Project description:In addition to altered gene expression, pathological cytoskeletal dynamics in the axon are another key intrinsic barrier for axon regeneration in the central nervous system (CNS). Here we showed that knocking out myosin IIA/B in retinal ganglion cells alone either before or after optic nerve crush induced significant optic nerve regeneration. Combined Lin28a overexpression and myosin IIA/B knockout led to additive promoting effect and long-distance axon regeneration. Immunostaining, RNA sequencing and western blot analyses revealed that myosin II deletion did not affect known axon regeneration signaling pathways or the expression of regeneration associated genes. Instead, it abolished the retraction bulb formation and significantly enhanced the axon extension efficiency. The study provided clear evidence that directly targeting neuronal cytoskeleton was sufficient to induce significant CNS axon regeneration, and combining altered gene expression in the soma and modified cytoskeletal dynamics in the axon was a promising approach for long-distance CNS axon regeneration
2020-03-22 | GSE147328 | GEO